Evidence map›Paper›PMID 21422186›Full record

ArticleInfection and immunity2011

The collagen-binding protein Cnm is required for Streptococcus mutans adherence to and intracellular invasion of human coronary artery endothelial cells.

Jacqueline Abranches, James H Miller, Alaina R Martinez, Patricia J Simpson-Haidaris, Robert A Burne, José A Lemos

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
11.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

110 citing papers in PubMed, 181 citations in OpenAlex.

  1. TheApplied and environmental microbiology · 2026
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  12. Binding of IgA1 and surface-expressed collagen-binding protein ofFrontiers in cellular and infection microbiology · 2025
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  13. MecA inmSphere · 2024
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  17. Inhibitory Effects of Shikonin Dispersion, an Extract ofInternational journal of molecular sciences · 2024
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  18. Roles ofFrontiers in microbiology · 2024
    Review
  19. Oral streptococci: modulators of health and disease.Frontiers in cellular and infection microbiology · 2024
    Review
  20. Amyloid Fibrils Produced byInternational journal of molecular sciences · 2023
    Article

50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Jacqueline AbranchesCenter for Oral Biology, University of Rochester Medical Center, Box 611, 601 Elmwood Ave., Rochester, NY 14642, USA. jacqueline_abranches@urmc.rochester.edu
James H Miller
Alaina R Martinez
Patricia J Simpson-Haidaris
Robert A Burne
José A Lemos
University of Rochester · USFlorida College · US

Funding

Training Program in Oral ScienceT90DE021985 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE, YULE, DAVID I · 2011 to 2021
$5.6M
TRAINING PROGRAM IN ORAL SCIENCET32DE007202 · NIDCR · UNIVERSITY OF ROCHESTER · PI QUIVEY, ROBERT G · 1990 to 2010
$5.5M
NIDCR NIH HHS T32 DE007202NIDCR NIH HHS T90 DE021985
6 · The paper itself

Abstract

Streptococcus mutans is considered the primary etiologic agent of dental caries, a global health problem that affects 60 to 90% of the population, and a leading causative agent of infective endocarditis. It can be divided into four different serotypes (c, e, f, and k), with serotype c strains being the most common in the oral cavity. In this study, we demonstrate that in addition to OMZ175 and B14, three other strains (NCTC11060, LM7, and OM50E) of the less prevalent serotypes e and f are able to invade primary human coronary artery endothelial cells (HCAEC). Invasive strains were also significantly more virulent than noninvasive strains in the Galleria mellonella (greater wax worm) model of systemic disease. Interestingly, the invasive strains carried an additional gene, cnm, which was previously shown to bind to collagen and laminin in vitro. Inactivation of cnm rendered the organisms unable to invade HCAEC and attenuated their virulence in G. mellonella. Notably, the cnm knockout strains did not adhere to HCAEC as efficiently as the parental strains did, indicating that the loss of the invasion phenotype observed for the mutants was linked to an adhesion defect. Comparisons of the invasive strains and their respective cnm mutants did not support a correlation between biofilm formation and invasion. Thus, Cnm is required for S. mutans invasion of endothelial cells and possibly represents an important virulence factor of S. mutans that may contribute to cardiovascular infections and pathologies.

Indexed as

Adhesins, BacterialAnimalsBacterial AdhesionBiofilmsCarrier ProteinsCoronary VesselsEndothelial CellsGene Knockout TechniquesGenes, BacterialHumansLarvaMothsReverse Transcriptase Polymerase Chain ReactionStreptococcal InfectionsStreptococcus mutansAdhesins, BacterialCarrier ProteinsCnm protein, Streptococcus mutans

Identifiers

PMID21422186
PMCPMC3125845
OpenAlexW2167552778

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.